author_facet Hoffmann, Ulrike
Sukhotinsky, Inna
Eikermann-Haerter, Katharina
Ayata, Cenk
Hoffmann, Ulrike
Sukhotinsky, Inna
Eikermann-Haerter, Katharina
Ayata, Cenk
author Hoffmann, Ulrike
Sukhotinsky, Inna
Eikermann-Haerter, Katharina
Ayata, Cenk
spellingShingle Hoffmann, Ulrike
Sukhotinsky, Inna
Eikermann-Haerter, Katharina
Ayata, Cenk
Journal of Cerebral Blood Flow & Metabolism
Glucose Modulation of Spreading Depression Susceptibility
Cardiology and Cardiovascular Medicine
Neurology (clinical)
Neurology
author_sort hoffmann, ulrike
spelling Hoffmann, Ulrike Sukhotinsky, Inna Eikermann-Haerter, Katharina Ayata, Cenk 0271-678X 1559-7016 SAGE Publications Cardiology and Cardiovascular Medicine Neurology (clinical) Neurology http://dx.doi.org/10.1038/jcbfm.2012.132 <jats:p> Spreading depression of Leão is an intense spreading depolarization (SD) wave associated with massive transmembrane ionic, water, and neurotransmitter shifts. Spreading depolarization underlies migraine aura, and occurs in brain injury, making it a potential therapeutic target. While susceptibility to SD can be modulated pharmacologically, much less is known about modulation by systemic physiological factors, such as the glycemic state. In this study, we systematically examined modulation of SD susceptibility by blood glucose in anesthetized rats under full physiological monitoring. Hyperglycemia and hypoglycemia were induced by insulin or dextrose infusion (blood glucose ~40 and 400 mg/dL, respectively). Spreading depolarizations were evoked by direct cortical electrical stimulation to determine the intensity threshold, or by continuous topical KCl application to determine SD frequency. Hyperglycemia elevated the electrical SD threshold and reduced the frequency of KCl-induced SDs, without significantly affecting other SD properties. In contrast, hypoglycemia significantly prolonged individual and cumulative SD durations, but did not alter the electrical SD threshold, or SD frequency, amplitude or propagation speed. These data show that increased cerebral glucose availability makes the tissue resistant to SD. </jats:p> Glucose Modulation of Spreading Depression Susceptibility Journal of Cerebral Blood Flow & Metabolism
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title Glucose Modulation of Spreading Depression Susceptibility
title_unstemmed Glucose Modulation of Spreading Depression Susceptibility
title_full Glucose Modulation of Spreading Depression Susceptibility
title_fullStr Glucose Modulation of Spreading Depression Susceptibility
title_full_unstemmed Glucose Modulation of Spreading Depression Susceptibility
title_short Glucose Modulation of Spreading Depression Susceptibility
title_sort glucose modulation of spreading depression susceptibility
topic Cardiology and Cardiovascular Medicine
Neurology (clinical)
Neurology
url http://dx.doi.org/10.1038/jcbfm.2012.132
publishDate 2013
physical 191-195
description <jats:p> Spreading depression of Leão is an intense spreading depolarization (SD) wave associated with massive transmembrane ionic, water, and neurotransmitter shifts. Spreading depolarization underlies migraine aura, and occurs in brain injury, making it a potential therapeutic target. While susceptibility to SD can be modulated pharmacologically, much less is known about modulation by systemic physiological factors, such as the glycemic state. In this study, we systematically examined modulation of SD susceptibility by blood glucose in anesthetized rats under full physiological monitoring. Hyperglycemia and hypoglycemia were induced by insulin or dextrose infusion (blood glucose ~40 and 400 mg/dL, respectively). Spreading depolarizations were evoked by direct cortical electrical stimulation to determine the intensity threshold, or by continuous topical KCl application to determine SD frequency. Hyperglycemia elevated the electrical SD threshold and reduced the frequency of KCl-induced SDs, without significantly affecting other SD properties. In contrast, hypoglycemia significantly prolonged individual and cumulative SD durations, but did not alter the electrical SD threshold, or SD frequency, amplitude or propagation speed. These data show that increased cerebral glucose availability makes the tissue resistant to SD. </jats:p>
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author Hoffmann, Ulrike, Sukhotinsky, Inna, Eikermann-Haerter, Katharina, Ayata, Cenk
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description <jats:p> Spreading depression of Leão is an intense spreading depolarization (SD) wave associated with massive transmembrane ionic, water, and neurotransmitter shifts. Spreading depolarization underlies migraine aura, and occurs in brain injury, making it a potential therapeutic target. While susceptibility to SD can be modulated pharmacologically, much less is known about modulation by systemic physiological factors, such as the glycemic state. In this study, we systematically examined modulation of SD susceptibility by blood glucose in anesthetized rats under full physiological monitoring. Hyperglycemia and hypoglycemia were induced by insulin or dextrose infusion (blood glucose ~40 and 400 mg/dL, respectively). Spreading depolarizations were evoked by direct cortical electrical stimulation to determine the intensity threshold, or by continuous topical KCl application to determine SD frequency. Hyperglycemia elevated the electrical SD threshold and reduced the frequency of KCl-induced SDs, without significantly affecting other SD properties. In contrast, hypoglycemia significantly prolonged individual and cumulative SD durations, but did not alter the electrical SD threshold, or SD frequency, amplitude or propagation speed. These data show that increased cerebral glucose availability makes the tissue resistant to SD. </jats:p>
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spelling Hoffmann, Ulrike Sukhotinsky, Inna Eikermann-Haerter, Katharina Ayata, Cenk 0271-678X 1559-7016 SAGE Publications Cardiology and Cardiovascular Medicine Neurology (clinical) Neurology http://dx.doi.org/10.1038/jcbfm.2012.132 <jats:p> Spreading depression of Leão is an intense spreading depolarization (SD) wave associated with massive transmembrane ionic, water, and neurotransmitter shifts. Spreading depolarization underlies migraine aura, and occurs in brain injury, making it a potential therapeutic target. While susceptibility to SD can be modulated pharmacologically, much less is known about modulation by systemic physiological factors, such as the glycemic state. In this study, we systematically examined modulation of SD susceptibility by blood glucose in anesthetized rats under full physiological monitoring. Hyperglycemia and hypoglycemia were induced by insulin or dextrose infusion (blood glucose ~40 and 400 mg/dL, respectively). Spreading depolarizations were evoked by direct cortical electrical stimulation to determine the intensity threshold, or by continuous topical KCl application to determine SD frequency. Hyperglycemia elevated the electrical SD threshold and reduced the frequency of KCl-induced SDs, without significantly affecting other SD properties. In contrast, hypoglycemia significantly prolonged individual and cumulative SD durations, but did not alter the electrical SD threshold, or SD frequency, amplitude or propagation speed. These data show that increased cerebral glucose availability makes the tissue resistant to SD. </jats:p> Glucose Modulation of Spreading Depression Susceptibility Journal of Cerebral Blood Flow & Metabolism
spellingShingle Hoffmann, Ulrike, Sukhotinsky, Inna, Eikermann-Haerter, Katharina, Ayata, Cenk, Journal of Cerebral Blood Flow & Metabolism, Glucose Modulation of Spreading Depression Susceptibility, Cardiology and Cardiovascular Medicine, Neurology (clinical), Neurology
title Glucose Modulation of Spreading Depression Susceptibility
title_full Glucose Modulation of Spreading Depression Susceptibility
title_fullStr Glucose Modulation of Spreading Depression Susceptibility
title_full_unstemmed Glucose Modulation of Spreading Depression Susceptibility
title_short Glucose Modulation of Spreading Depression Susceptibility
title_sort glucose modulation of spreading depression susceptibility
title_unstemmed Glucose Modulation of Spreading Depression Susceptibility
topic Cardiology and Cardiovascular Medicine, Neurology (clinical), Neurology
url http://dx.doi.org/10.1038/jcbfm.2012.132